One of the largest studies to date could hold the key to understanding Alzheimer's disease - and how to stop it.

According to the Centers for Disease Control, more than 6.7 million people in the U.S. are living with Alzheimer’s disease, and that number is expected to double by 2060. It remains the leading cause of dementia, and there is no known cure. However, years of research have led to numerous advancements in treatment, including a recent decade-long study that many believe could lead to new therapies to slow progression of Alzheimer’s disease.

“In the next 5-10 years, this research will continue to progress and could be crucial in the development of a multi-faceted treatment approach to improve symptoms related to Alzheimer’s and slow the progression of the disease,” says Mark Friedman, DO, board-certified neurologist at the Memory and Disorder Clinic at SMH. “This is very hopeful.”

What is Alzheimer's Disease: Amyloid Plaque & Tangled Tau

Alzheimer's disease is a progressive neurological condition that results in cognitive decline and memory deterioration. It is the leading cause of dementia in the world today.

For decades, physicians and research scientists have studied the disease in hopes of finding a treatment or a therapy that could forestall memory loss or preserve cognitive function. Much of this research has been focused on what are called amyloid plaques.

Amyloid plaques are sticky abnormal protein deposits that accumulate in the brain. In a healthy brain, these proteins are cleared out naturally during sleep. Alzheimer's disease prevents the brain from getting rid of these proteins. The proteins become sticky gunk that builds up, disrupts brain function, and causes cell death.

For a long time, this plaque was believed to be the main culprit behind Alzheimer’s disease.

However, recent research suggests that a little protein called tau may be just as responsible for the progression of the disease.

Tau is a protein in the brain that primarily helps to stabilize the internal cell structure, but also assists in memory, sleep cycle, and cellular signaling. In Alzheimer's patients, tau proteins can detach and form neurofibrillary tangles, twisted clumps of protein that build inside the brain, causing cell death. It's thought that the location and amount of these tau tangles directly affect memory and cognitive deterioration.

“Stopping the spread of tau could significantly slow the progression of the disease,” says Dr. Friedman, “and potentially improve memory function.”

Untangling Tau: Mapping the Brain & Tracking the Spread

Until recently, researchers knew that tau tangles spread through the brain but did not know how the spread occurred. They suspected this could be the missing component preventing effective treatments from being developed.

To answer that question, researchers conducted the largest investigation of tau bioactivity to date, analyzing brain samples from both those with Alzheimer's and those without. Using what is called functional magnetic resonance imaging, or fMRI, researchers actually mapped each individual's unique brain activity, looking for patterns. The study explored two brain regions: the lower temporal lobe, which is responsible for memory recall, and the upper frontal lobe, which is responsible for working memory and complex thought.

Researchers found that the tau protein follows a predictable path in the brain, spreading from the temporal lobe to the frontal lobe, mirroring the progression of Alzheimer’s disease symptoms, from early memory problems to more advanced cognitive impairment.

More surprisingly, the study revealed that tau tangles spread through living, connected neurons, surfing our thoughts through firing synapses. Previously, tau was believed to travel through damaged or dead neurons.

This means every person’s unique brain connectivity could determine how far and fast the disease progresses.

"If there's a way to predict the rate of progression, then there's a way to target treatments more quickly and in a more focused manner," says Dr. Friedman. "It may result in personalized treatments that target the tau protein in addition to the anti-amyloid therapies we have now."

 

 

 

Written by Sarasota Memorial Contributing Writer Grace Walker, a student of Mass Communications at the University of South Florida - Tampa.